Circulating autoantibodies are responsible for much of the pathogenesis associated with a number of autoimmune diseases including, but not limited to, systemic lupus erythematosus (SLE), autoimmune myocarditis, immune complex mediated kidney disease, rheumatoid arthritis, myasthenia gravis, autoimmune anemias, Sjogren's Syndrome, idiopathic thrombocytopenic purpura, various forms of vasculitis, and at least some of the cellular cytotoxicity accompanying Acquired Immune Deficiency Syndrome (AIDS).
Efforts to treat autoantibody-mediated disorders have been only partially successful. Many of the past developed therapies have been based on the use of general immunosuppressive measures, through drugs or therapeutic monoclonal antibodies designed to completely abrogate antibody production. However, to date, a successful treatment has not been designed which targets the specific autoantibodies.
Plasmapheresis, which is designed to remove all the circulating antibodies, has been attempted, but only with limited success. In recent years, a variety of extracorporeal immunoabsorption procedures have been attempted. These procedures are more specific, and attempt to remove only the pathogenic autoantibodies. This involves allowing the blood or plasma to flow over matrices outside the body which contain the autoantigen which is the natural target of the autoantibodies. These methods are slow, invasive, and expensive, and are associated with several technical problems including the need to perform the procedures repeatedly because of their quantitative inefficiency. The complication of complement activation on the matrices exists. Overall, therapeutic successes have been modest, at best.
Another general, non-specific approach involves aggressive immunosuppressive therapy with corticosteroids, and cytotoxic and nonsteroidal anti-inflammatory drugs. Although in many instances clinical improvements have been obtained, there continues to be significant morbidity and mortality in autoimmune diseases despite these medications.
Therefore, notwithstanding these advances in autoimmune therapy, there remains to be seen an internal therapy which is specific for the target pathogenic autoantibody and which is both fast and quantitative.